Difference between revisions of "Vomiting"

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* Has potentially lethal effects in the monogastric animal.
==Overview==
 
  
Vomiting has potentially lethal effects in the monogastric animal. The effects are listed below. It is clinically important to differentiate vomiting from [[Regurgitation|regurgitation]], as clients can often confuse these clinical signs and the two have very different aetiologies.<br>
 
  
 
===Water Loss===
 
===Water Loss===
  
Fluid loss is evident as an increased PCV or haematocrit, an increased total protein concentration or a prerenal [[Azotaemia|azotaemia]].  
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* Fluid loss is evident as:
 +
*# An increased PCV or haematocrit.
 +
*# An increased total protein concentration.
 +
*# A prerenal azotaemia.  
 +
 
  
 
===Gastric Electrolyte Loss===
 
===Gastric Electrolyte Loss===
  
The main losses are of H<sup>+</sup> and Cl<sup>-</sup>, and also K<sup>+</sup>. [[:Category:Electrolytes|Electrolyte]] loss can potentially cause metabolic alkalosis, although this is only likely with disease which stops at the pylorus, e.g.: pyloric outflow obstruction. In cases where '''mild alkalosis''' occurs, homeostatic mechanisms produce a more alkaline urine to restore normal body pH. However, in '''severe metabolic alkalosis''' with marked dehydration, acidic urine may be produced. This is termed '''paradoxical aciduria'''. Because vomiting induces hypokalaemia, there is an overriding stimulus in the kidney for Na<sup>+</sup> (and therefore water) retention. Na+ can only be resorbed in exchange for H+, H+<sup>+</sup> is therefore excreted in the urine, causing it to be acidic. Vomiting also induces '''hypochloraemia''', meaning bicarbonate rather than chloride is resorbed with the Na+ to maintain electrical neutrality. This perpetuates the alkalosis.  
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* The main losses are of H<sup>+</sup> and Cl<sup>-</sup>, and also K<sup>+</sup>
 +
* Can potentially cause metabolic alkalosis, although this is only likely with disease which stops at the pylorus, e.g.: pyloric outflow obstruction.  
 +
** In cases where mild alkalosis occurs, homeostatic mechanisms produce a more alkaline urine to restore normal body pH.
 +
** However, in severe metablolic alkalosis with marked dehydration, acidic urine may be produced- this is termed '''paradoxical aciduria'''.
 +
*** Because [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomiting]] induceses hypokalaemia, there is an overriding stimulus in the kidney for Na<sup>+</sup> (and therefore water) retention.  
 +
*** Na+ can only be resorbed in exchange for H+  
 +
**** H<sup>+</sup> is therefore excreted in the urine, causing it to be acidic.
 +
*** [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] also induces hypochloraemia, meaning bicarbonate rather than chloride is resorbed with the Na+ to maintain electrical neutrality
 +
**** This perpetuates the alkalosis.
 +
* [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] does not occur in the ruminant although [[The Abomasum - Anatomy & Physiology|abomasal]] content may reflux into the [[Stomach and Abomasum - Anatomy & Physiology|forestomachs]].
 +
** Sequestration of secretions in the [[The Abomasum - Anatomy & Physiology|abomasum]] will have similar effects to pyloric outflow obstruction with [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomiting]] in the monogastric animal.
 +
*** e.g. abomasal torsion
 +
*** Causes dehydration, hypochloraemia, hypokalaemia and metabolic alkalosis.
 +
 
 +
 
 +
* Lesions in the [[Small Intestine - Anatomy & Physiology|small intestine]] can also lead to [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomiting]]
 +
** Both gastric acid and pancreatic and intestinal bicarbonate secretions are lost
 +
*** Animal consequently has a normal pH or may even be acidotic.
  
Vomiting does not occur in the ruminant although [[Abomasum - Anatomy & Physiology|abomasal]] content may reflux into the [[Ruminant Stomach - Anatomy & Physiology|forestomachs]]. Sequestration of secretions in the [[Abomasum - Anatomy & Physiology|abomasum]] will have similar effects to pyloric outflow obstruction with vomiting in the monogastric animal, e.g. [[Displaced Abomasum|abomasal torsion]]. It also causes dehydration, hypochloraemia, hypokalaemia and metabolic alkalosis. Lesions in the [[Small Intestine Overview - Anatomy & Physiology|small intestine]] can also lead to vomiting. Both gastric acid and pancreatic and intestinal bicarbonate secretions are lost, the animal consequently has a normal pH or may even be '''acidotic'''.
 
  
 
==The Vomit Reflex==
 
==The Vomit Reflex==
[[Image:The Vomit Reflex Pathway.jpg|right|thumb|250px|The Vomit Reflex - Copyright nabrown RVC]]
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[[Image:The Vomit Reflex Pathway.jpg|right|thumb|150px|The Vomit Reflex - Copyright nabrown RVC]]
'''Emesis''' is the process of vomiting. Persistent vomiting can be exhausting and can lead to [[Essential Ion and Compound Balance and Homeostasis - Anatomy & Physiology#Alkalosis|metabolic alkalosis]], [[Dehydration|dehydration]] and electrolyte imbalances which may require [[Principles of Fluid Therapy|fluid therapy]]. Extreme cases of persistent vomiting can lead to [[Shock|shock]].  
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*Emesis is the process of vomiting
 +
 
 +
*Persistent vomiting can be exhausting and can lead to metabolic alkalosis, dehydration and electrolyte inbalances which may require fluid therapy
 +
 
 +
*Extreme cases of persistent vomiting can lead to shock
 +
 
 +
*Retching involves the abdominal and chest walls contracting
 +
 
 +
*Vomiting includes retching and the action of the diaphragm
 +
 
 +
*Diaphragm moves caudal to open the cardia
 +
 
 +
*Gastrointestinal tract have protective stimuli to recognise harmful products ingested. The mechanoreceptors and chemoreceptors respond using viscerent afferent pathways.
  
Vomiting includes retching and the action of the [[Diaphragm - Anatomy & Physiology|diaphragm]]. The diaphragm moves caudal to open the cardia and retching involves the abdominal and chest walls contracting. The gastrointestinal tract has protective stimuli to recognise harmful products ingested. The mechanoreceptors and chemoreceptors respond using visceral afferent pathways. The [[Hindbrain - Anatomy & Physiology#Medulla Oblongata|medulla]] co-ordinates the process and the chemoreceptive trigger zone in the 4th ventricle responds to blood and [[Cerebral Spinal Fluid - Anatomy & Physiology|CSF]]. Inputs are also received from the [[Ear - Anatomy & Physiology#Inner Ear|inner ear]] and higher centres.
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*Medulla co-ordinates process
  
Emetic agents can be used in cases of gastric obstruction and to remove non-corrosive poisons from the stomach (for corrosive poisons charcoal can be used which will help adsorb the substance and decrease its absorption into the gastrointestinal tract).
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*Chemoreceptive trigger zone in the 4th ventricle responds to blood and CSF
  
===[[Emetics and Anti-Emetic Drugs|Emetic agents]]===
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*Inputs also from inner ear and higher centres
  
Drugs cause emesis by irritating the gastric mucosa. Emetic drugs include the following:
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*Emetic agents can be used in cases of gastric obstruction and to remove non-corrosive poisons from the stomach (for corrosive poisons charcoal can be used which will help adsorb the substance and decrease its absorbtion into the GIT)
  
*Histamine
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*For more information on emetic and anti-emetic drugs click [[Emetics and Anti-Emetic Drugs|here]]
*ACh
 
*Dopamine
 
*Catecholamines
 
*5-hydroxytryptamine
 
*Substance P
 
*Enkephalins
 
*NK1 receptor agonists
 
  
===[[Emetics and Anti-Emetic Drugs|Anti-emetic agents]]===
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===Emetic agents===
 +
*Drugs cause emesis by irritating the gastric mucosa
 +
**Histamine
 +
**ACh
 +
**Dopamine
 +
**Catecholamines
 +
**5-hydroxytryptamine
 +
**Substance P
 +
**Enkephalins
 +
**NK1 receptor agonists
  
Anti-emetic agents can be used to treat motion sickness and to treat or prevent vomiting. They include the following:
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===Anti-emetic agents===
*Dopamine (D2) receptor antagonists
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*Anti-emetic agents can be used to treat motion sickness and to treat or prevent vomiting
*5-hydroxytryptamine antagonists
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**Dopamine (D2) receptor antagonists
*NK1 receptor antagonists
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**5-hydroxytryptamine antagonists
*Muscarinic receptor antagonists
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**NK1 receptor antagonists
*Histamine (H1) receptor antagonists
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**Muscarinic receptor antagonists
*[[Gastroprotective Drugs|Gastroprotective agents]]
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**Histamine (H1) receptor antagonists
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**Gastroprotective agents
  
{{OpenPages}}
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[[Category:Control of Feeding]]
[[Category:Feeding Control]]
 
[[Category:A&P Done]]
 

Revision as of 15:58, 2 September 2010

  • Has potentially lethal effects in the monogastric animal.


Water Loss

  • Fluid loss is evident as:
    1. An increased PCV or haematocrit.
    2. An increased total protein concentration.
    3. A prerenal azotaemia.


Gastric Electrolyte Loss

  • The main losses are of H+ and Cl-, and also K+
  • Can potentially cause metabolic alkalosis, although this is only likely with disease which stops at the pylorus, e.g.: pyloric outflow obstruction.
    • In cases where mild alkalosis occurs, homeostatic mechanisms produce a more alkaline urine to restore normal body pH.
    • However, in severe metablolic alkalosis with marked dehydration, acidic urine may be produced- this is termed paradoxical aciduria.
      • Because vomiting induceses hypokalaemia, there is an overriding stimulus in the kidney for Na+ (and therefore water) retention.
      • Na+ can only be resorbed in exchange for H+
        • H+ is therefore excreted in the urine, causing it to be acidic.
      • Vomiting also induces hypochloraemia, meaning bicarbonate rather than chloride is resorbed with the Na+ to maintain electrical neutrality
        • This perpetuates the alkalosis.
  • Vomiting does not occur in the ruminant although abomasal content may reflux into the forestomachs.
    • Sequestration of secretions in the abomasum will have similar effects to pyloric outflow obstruction with vomiting in the monogastric animal.
      • e.g. abomasal torsion
      • Causes dehydration, hypochloraemia, hypokalaemia and metabolic alkalosis.


  • Lesions in the small intestine can also lead to vomiting
    • Both gastric acid and pancreatic and intestinal bicarbonate secretions are lost
      • Animal consequently has a normal pH or may even be acidotic.


The Vomit Reflex

The Vomit Reflex - Copyright nabrown RVC
  • Emesis is the process of vomiting
  • Persistent vomiting can be exhausting and can lead to metabolic alkalosis, dehydration and electrolyte inbalances which may require fluid therapy
  • Extreme cases of persistent vomiting can lead to shock
  • Retching involves the abdominal and chest walls contracting
  • Vomiting includes retching and the action of the diaphragm
  • Diaphragm moves caudal to open the cardia
  • Gastrointestinal tract have protective stimuli to recognise harmful products ingested. The mechanoreceptors and chemoreceptors respond using viscerent afferent pathways.
  • Medulla co-ordinates process
  • Chemoreceptive trigger zone in the 4th ventricle responds to blood and CSF
  • Inputs also from inner ear and higher centres
  • Emetic agents can be used in cases of gastric obstruction and to remove non-corrosive poisons from the stomach (for corrosive poisons charcoal can be used which will help adsorb the substance and decrease its absorbtion into the GIT)
  • For more information on emetic and anti-emetic drugs click here

Emetic agents

  • Drugs cause emesis by irritating the gastric mucosa
    • Histamine
    • ACh
    • Dopamine
    • Catecholamines
    • 5-hydroxytryptamine
    • Substance P
    • Enkephalins
    • NK1 receptor agonists

Anti-emetic agents

  • Anti-emetic agents can be used to treat motion sickness and to treat or prevent vomiting
    • Dopamine (D2) receptor antagonists
    • 5-hydroxytryptamine antagonists
    • NK1 receptor antagonists
    • Muscarinic receptor antagonists
    • Histamine (H1) receptor antagonists
    • Gastroprotective agents